Zinc deficiency and advanced liver fibrosis among HIV and hepatitis C co-infected anti-retroviral naïve persons with alcohol use in Russia.


Journal

PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081

Informations de publication

Date de publication:
2019
Historique:
received: 05 02 2019
accepted: 11 06 2019
entrez: 28 6 2019
pubmed: 28 6 2019
medline: 14 2 2020
Statut: epublish

Résumé

Liver disease in people living with HIV co-infected with hepatitis C virus is a source of morbidity and mortality in Russia. HIV accelerates liver fibrosis in the setting of HCV co-infection and alcohol use. Zinc deficiency is common among people living with HIV and may be a factor that facilitates the underlying mechanisms of liver fibrosis. We investigated the association between zinc deficiency and advanced liver fibrosis in a cohort of HIV/HCV co-infected persons reporting heavy drinking in Russia. This is a secondary data analysis of baseline data from 204 anti-retroviral treatment naïve HIV/HCV co-infected Russians with heavy drinking that were recruited into a clinical trial of zinc supplementation. The primary outcome of interest in this cross-sectional study was advanced liver fibrosis. Zinc deficiency, the main independent variable, was defined as plasma zinc <0.75 mg/L. Exploratory analyses were performed examining continuous zinc levels and fibrosis scores. Analyses were conducted using multivariable regression models adjusted for potential confounders. The prevalence of advanced liver fibrosis was similar for those with zinc deficiency compared to those with normal zinc levels, (27.7% vs. 23.0%, respectively). We did not detect an association between zinc deficiency and advanced liver fibrosis in the adjusted regression model (aOR: 1.28, 95% CI: 0.62-2.61, p = 0.51) nor in exploratory analyses. In this cohort of Russians with HIV/HCV co-infection, who are anti-retroviral treatment naïve and have heavy alcohol use, we did not detect an association between zinc deficiency or zinc levels and advanced liver fibrosis.

Sections du résumé

BACKGROUND AND AIMS
Liver disease in people living with HIV co-infected with hepatitis C virus is a source of morbidity and mortality in Russia. HIV accelerates liver fibrosis in the setting of HCV co-infection and alcohol use. Zinc deficiency is common among people living with HIV and may be a factor that facilitates the underlying mechanisms of liver fibrosis. We investigated the association between zinc deficiency and advanced liver fibrosis in a cohort of HIV/HCV co-infected persons reporting heavy drinking in Russia.
METHODS
This is a secondary data analysis of baseline data from 204 anti-retroviral treatment naïve HIV/HCV co-infected Russians with heavy drinking that were recruited into a clinical trial of zinc supplementation. The primary outcome of interest in this cross-sectional study was advanced liver fibrosis. Zinc deficiency, the main independent variable, was defined as plasma zinc <0.75 mg/L. Exploratory analyses were performed examining continuous zinc levels and fibrosis scores. Analyses were conducted using multivariable regression models adjusted for potential confounders.
RESULTS
The prevalence of advanced liver fibrosis was similar for those with zinc deficiency compared to those with normal zinc levels, (27.7% vs. 23.0%, respectively). We did not detect an association between zinc deficiency and advanced liver fibrosis in the adjusted regression model (aOR: 1.28, 95% CI: 0.62-2.61, p = 0.51) nor in exploratory analyses.
CONCLUSIONS
In this cohort of Russians with HIV/HCV co-infection, who are anti-retroviral treatment naïve and have heavy alcohol use, we did not detect an association between zinc deficiency or zinc levels and advanced liver fibrosis.

Identifiants

pubmed: 31246992
doi: 10.1371/journal.pone.0218852
pii: PONE-D-19-03534
pmc: PMC6597160
doi:

Substances chimiques

Zinc J41CSQ7QDS

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

e0218852

Subventions

Organisme : NIAAA NIH HHS
ID : U24 AA020779
Pays : United States
Organisme : NIAAA NIH HHS
ID : U01 AA021989
Pays : United States
Organisme : NIAID NIH HHS
ID : T32 AI052074
Pays : United States
Organisme : NIAAA NIH HHS
ID : U01 AA020780
Pays : United States
Organisme : NIAAA NIH HHS
ID : U24 AA020778
Pays : United States
Organisme : NIAID NIH HHS
ID : P30 AI042853
Pays : United States

Déclaration de conflit d'intérêts

The authors have declared that no competing interests exist.

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Auteurs

Joshua A Barocas (JA)

Section of Infectious Diseases, Boston Medical Center, Boston, Massachusetts, United States of America.
Boston University School of Medicine, Boston, Massachusetts, United States of America.

Kaku So-Armah (K)

Boston University School of Medicine, Boston, Massachusetts, United States of America.

Debbie M Cheng (DM)

Boston University School of Public Health, Boston, Massachusetts, United States of America.

Dmitry Lioznov (D)

First Pavlov State Medical University, St. Petersburg, Russia.
Smoridintsev Research Institute of Influenza, St. Petersburg, Russia.

Marianna Baum (M)

Florida International University, Robert Stempel College of Public Health and Social Work, Miami, Florida, United States of America.

Kerrin Gallagher (K)

Boston University School of Public Health, Boston, Massachusetts, United States of America.

Daniel Fuster (D)

Hospital Universitari Germans Trias I Pujol, Badalona, Spain.

Natalia Gnatienko (N)

Section of General Internal Medicine, Boston Medical Center, Boston, Massachusetts, United States of America.

Evgeny Krupitsky (E)

First Pavlov State Medical University, St. Petersburg, Russia.
V.M. Bekhterev National Medical Research Center for Psychiatry and Neurology, St. Petersburg, Russia.

Matthew S Freiberg (MS)

Vanderbilt University Medical Center, Nashville, Tennessee, United States of America.

Jeffrey H Samet (JH)

Boston University School of Medicine, Boston, Massachusetts, United States of America.
Section of General Internal Medicine, Boston Medical Center, Boston, Massachusetts, United States of America.

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